Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve recurrent stone formers with hyperoxaluria were administered pyridoxine-HCl (10 mg/day) daily for a period of 180 days. The pyridoxine status of the patients, as assessed by their erythrocyte transaminase activation indexes, improved significantly (p less than 0.001) after 180 days of supplementation as compared with the basal levels. Although urinary oxalate decreased significantly (p less than 0.05) by the 90th day of pyridoxine therapy, other parameters, e.g., urinary calcium, phosphorus, and creatinine, remained unaltered. Significant correlation was observed between erythrocyte glutamate pyruvate transaminase (EGPT) or erythrocyte glutamate oxaloacetate transaminase (EGOT) activation index and urinary oxalate excretion (p less than 0.01). Pyridoxine in low doses (10 mg/day) is of therapeutic value for hyperoxaluric stone formers.
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PMID:Effect of pyridoxine supplementation on recurrent stone formers. 714 62

Proteins are thought to play a major role in stone formation and structurally abnormal proteins have been reported to be present in the urine of stone formers. This study was aimed to determine whether hyperoxaluria modifies the kinetic properties of urinary inhibitory proteins. Hyperoxaluria was induced by feeding 1% ethylene glycol to rats. Oxalate, uric acid and calcium excretion were increased progressively during hyperoxaluria, while magnesium level was decreased. Urinary proteins were separated on a DEAE-cellulose column by eluting with stepwise increasing salt concentration in 0.05 M Tris-HCl buffer (pH 7.0). Each protein fraction was studied for its crystallization inhibitory potential by the spectrophotometric method. The protein eluted in 0.3 M NaCl containing buffer had the maximal nucleation as well as inhibitory activity. The protein had a molecular weight of 45 kD. In hyperoxaluria, the urinary excretion of this protein significantly increased. In the crystal growth assay, the control rat 45-kD protein inhibited nucleation by 75% and aggregation by 100%. In contrast, it is very interesting to note that the protein derived from 28th day hyperoxaluric urine, behaved as a promoter of nucleation (-113%, percentage inhibition) and weak inhibitor of aggregation (28%). A significantly high negative correlation (r = -0.97) between oxalate excretion and the inhibitory activity of the 45-kD protein was observed suggesting a modification of the protein by oxalate.
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PMID:Effect of hyperoxaluria on the inhibitory activity of a 45-kD urinary protein. 1181 6

Annual incidences of kidney stones are about 0.1-0.4% of the population, and lifetime prevalences in the USA and Europe range between 8 and 15%. Kidney stones occur more frequently with increasing age and among men. Within ten years, the disease usually recurs in more than 50% of patients. Nowadays, about 85% of all kidney stones contain calcium salts (calcium oxalate and/or calcium phosphate) as their main crystalline components. Because human urine is commonly supersaturated with respect to calcium salts as well as to uric acid, crystalluria is very common, i.e. healthy people excrete up to ten millions of microcrystals every day. Recurrent stone formers appear to excrete lower amounts or structurally defective forms of crystallization inhibitors which allows for the formation of large crystal aggregates as precursors of stones. Alternatively, crystal adhesion to urothelial surfaces may be enhanced in stone formers. Medical treatment of renal colic is based on nonsteroidal antiinflammatory drugs, because prostaglandins appear to play a crucial role in the pathophysiology of pain during ureteral obstruction. In addition, centrally acting analgesics such as pethidine-HCl may be required in many cases. The administration of high amounts (3-4 liters/day) of intravenous fluids should be abandoned, since it may raise intraureteral pressure whereby pain increases and kidney pelvis or fornices may rupture. All first-stone formers should undergo a simple basic evaluation, including stone analysis (x-ray diffraction or infrared spectrometry), serum values of ionized calcium (alternatively: total calcium and albumin) and creatinine, urinalysis and repeated measurements of fasting urine pH in order to detect urinary acidification disorders or low urine pH. In high-risk patients with as first stone episode (i.e. strongly positive family history, inflammatory bowel disease, short-bowel syndrome, nephrocalcinosis, bilateral stones, hypercalcemia, renal tubular acidosis, airline pilots) as well as in all recurrent stone formers, an extended metabolic evaluation should be performed. Two 24-hurines should be collected on free-choice diet not prior to three months after stone passage or urological intervention. Analysis includes measurements of volume, creatinine, calcium, oxalate, uric acid and citrate; sodium and urea as markers of salt and protein consumption are optional but clinically very helpful. Since hypercalciuria is of much less importance than increases in urinary oxalate, therapeutic efforts should primarily focus on lowering urinary oxalate excretion. Sufficient calcium intake, i.e. 1200 mg per day, is crucial, because it allows for binding of oxalate at the intestinal level whereby increases of urinary oxalate (reciprocal hyperoxaluria) can be avoided. Excess intake of flesh protein (meat, fish, poultry) is lithogenic since it increases urinary calcium, oxalate and uric acid, and lower citrate. On the other hand, a diet rich in alkali (vegetables, fruit) is associated with a lower risk of stone formation. A "common sense diet" containing sufficient amounts of fluids, 1200 mg of calcium per day and reduced amounts of flesh protein as well as salt is able to reduce the 5-year stone recurrence rate in calcium stone formers by 50%. The scientific evidence for drug treatment (thiazides, alkali citrate) is rather poor: the most widely quoted randomized thiazide trial included only 42 patients of whom 36% left the protocol prematurely, whereas 36-48% of patients included in three randomized studies with alkali citrate suffered from undesirable side-effects; nevertheless, citrate therapy reduced the stone recurrence rate by 38%, compared with 22% in patients on placebo treatment (p < 0.0005).
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PMID:[Pathophysiology, diagnosis and conservative therapy in calcium kidney calculi]. 1264 86

This study was done to resolve published discrepancies in oxalate excretion between humans and rats and to characterize oxalate partitioning in rats during persistent severe hyperoxaluria, such as that seen in many bariatric patients. Osmotic minipumps dispensing 360 micromole/day KOx + 3.9 +/- 0.14 microCi/day (14)C-oxalate were implanted subcutaneously. All excreta were collected. Rats were killed on day 13 and carcasses were dissected, ground, dissolved in HCl, and subjected to scintillation counting, and 92.1 +/- 3.9% of total oxalate administered was recovered. This was partitioned among the skin complex (38.2 +/- 7.7%), carcass complex (24.5 +/- 5.9%), and excreta (29.5 +/- 1.9%). The distribution of oxalate in the skin and carcass complexes led us to infer that only 29.5 +/- 1.9% of the administered oxalate entered the circulation. Of the circulated oxalate, 98.4 +/- 0.4% was excreted (total urine 78.9 +/- 1.7%; raw feces 21.0 +/- 1.7%). Thus, most oxalate that does enter the circulation is promptly excreted in rats, as in humans. Consequently, even after a large, persistent oxalate challenge, very little oxalate had accumulated in the internal organs, muscle, and skeleton. Unlike humans, however, rats excrete a significant fraction of oxalate in the feces.
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PMID:Partitioning of 14C-oxalate excretion in rats during a persistent oxalate challenge. 1892 24